Part I: Hodgkin's lymphoma - Molecular biology of Hodgkin and Reed-Sternberg cells

Lancet Oncology

Volumn 5, Issue 1, 2004, Pages 11-18

  Thomas, Roman K ^a   Re, Daniel ^a   Wolf, Jürgen ^a   Diehl, Volker ^a  

^a UNIVERSITY OF COLOGNE   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

B LYMPHOCYTE RECEPTOR; CD20 ANTIGEN; CD79A ANTIGEN; FAS ANTIGEN; IMMUNOGLOBULIN; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; PROTEIN BCL 10; PROTEIN BCL 6; PROTEIN MLH1; PROTEIN MSH2; PROTEIN P53; VIRUS DNA;

APOPTOSIS; B LYMPHOCYTE; BINDING AFFINITY; CANCER GROWTH; CANCER RESEARCH; CHROMOSOME 12Q; CHROMOSOME 2P; CHROMOSOME 9P; CHROMOSOME ABERRATION; ENVIRONMENTAL FACTOR; EPSTEIN BARR VIRUS; GENE EXPRESSION; GENE MUTATION; GENE REARRANGEMENT; GENETIC TRANSCRIPTION; GERMINAL CENTER; HODGKIN DISEASE; HUMAN; MOLECULAR BIOLOGY; MOLECULAR MECHANICS; ONCOVIRINAE; PHENOTYPE; POLIOMYELITIS VIRUS; PRIORITY JOURNAL; PROTEIN FUNCTION; RECEPTOR BINDING; REED STERNBERG CELL; REVIEW; SIGNAL TRANSDUCTION; STEM CELL;

EID: 0347286872     PISSN: 14702045     EISSN: None     Source Type: Journal    
DOI: 10.1016/S1470-2045(03)01319-6     Document Type: Review

References (76)

1. Jaffe ES, Harris NL, Stein H, Vardiman JW. Tumours of haematopoietic and lymphoid tissues. Lyon: IARC Press, International Agency for Research on Cancer, 2001; 175-176.
2. Falini B, Bigerna B, Pasqualucci, L et al. Distinctive expression pattern of the BCL-6 protein in nodular lymphocyte predominance Hodgkin's disease. Blood 1996; 87: 465-71.
3. Küppers R, Rajewsky K, Zhao M, et al. Hodgkin disease: Hodgkin and Reed-Sternberg cells picked from histological sections show clonal immunoglobulin gene rearrangements and appear to be derived from B cells at various stages of development. Proc Natl Acad Sci USA 1994; 91: 10962-66.
4. Kanzler H, Küppers R, Hansmann ML, et al. Hodgkin and Reed-Sternberg cells in Hodgkin's disease represent the outgrowth of a dominant tumor clone derived from (crippled) germinal center B cells. J Exp Med 1996; 184: 1495-505.
5. Müschen M, Rajewsky K, Brauninger A, et al. Rare occurrence of classical Hodgkin's disease as a T cell lymphoma. J Exp Med 2000; 191: 387-94.
6. Seitz V, Hummel M, Marafioti T, et al. Detection of clonal T-cell receptor gamma-chain gene rearrangements in Reed-Sternberg cells of classic Hodgkin disease. Blood 2000; 95: 3020-24.
7. Braeuninger A, Küppers R, Strickler JG, et al. Hodgkin and Reed-Sternberg cells in lymphocyte predominant Hodgkin disease represent clonal populations of germinal center-derived tumor B cells. Proc Natl Acad Sci USA 1997; 94: 9337-42.
8. Marafioti T, Hummel M, Anagnostopoulos I, et al. Origin of nodular lymphocyte-predominant Hodgkin's disease from a clonal expansion of highly mutated germinal-center B cells. N Engl J Med 1997; 337: 453-58.
9. Rajewsky K. Clonal selection and learning in the antibody system. Nature 1996; 381: 751-58.
10. Martinez-Valdez H, Guret C, de Bouteiller O, et al. Human germinal center B cells express the apoptosis-inducing genes Fas, c-myc, P53, and Bax but not the survival gene bcl-2. J Exp Med 1996; 183: 971-77.
11. Hennino A, Berard M, Krammer PH, et al. FLICE-inhibitory protein is a key regulator of germinal center B cell apoptosis. J Exp Med 2001; 193: 447-58.
12. van Eijk M, Medema JP, de Groot C, et al. Cutting edge: cellular Fas-associated death domain-like IL-1-converting enzyme-inhibitory protein protects germinal center B cells from apoptosis during germinal center reactions. J Immunol 2001; 166: 6473-76.
13. Marafioti T, Hummel M, Foss HD, et al. Hodgkin and Reed-Sternberg cells represent an expansion of a single clone originating from a germinal center B-cell with functional immunoglobulin gene rearrangements but defective immunoglobulin transcription. Blood 2000; 95: 1443-50.
14. Jox A, Zander T, Küppers R, et al. Somatic mutations within the untranslated regions of rearranged Ig genes in a case of classical Hodgkin's disease as a potential cause for the absence of Ig in the lymphoma cells. Blood 1999; 93: 3964-72.
15. Theil J, Laumen H, Marafioti, T et al. Defective octamer-dependent transcription is responsible for silenced immunoglobulin transcription in Reed-Sternberg cells. Blood 2001; 97: 3191-96.
16. Re D, Staratschek-Jox A, Holtick U, et al. Deregulation of immunoglobulin gene transcription in the Hodgkin-Reed Sternberg cell line L1236. Br J Haematol 2001; 115: 326-28.
17. Re D, Muschen M, Ahmadi T, et al. Oct-2 and Bob-1 deficiency in Hodgkin and Reed Sternberg cells. Cancer Res 2001; 61: 2080-84.
18. Stein H, Marafioti T, Foss HD, et al. Down-regulation of BOB.1/OBF.1 and Oct2 in classical Hodgkin disease but not in lymphocyte predominant Hodgkin disease correlates with immunoglobulin transcription. Blood 2001; 97: 496-501.
19. Torlakovic E, Tierens A, Dang HD, et al. The transcription factor PU.1, necessary for B-cell development is expressed in lymphocyte predominance, but not classical Hodgkin's disease. Am J Pathol 2001; 159: 1807-14.
20. Schwering I, Bräuninger A, Klein U, et al. Loss of the B-lineage-specific gene expression program in Hodgkin and Reed-Sternberg cells of Hodgkin lymphoma. Blood 2003; 101: 1505-12.
21. Küppers R, Brauninger A, Müschen M, et al. Evidence that Hodgkin and Reed-Sternberg cells in Hodgkin disease do not represent cell fusions. Blood 2001; 97: 818-21.
22. Re D, Hofmann A, Wolf J, et al. Cultivated H-RS cells are resistant to CD95L-mediated apoptosis despite expression of wild-type CD95. Exp Hematol 2000; 28: 31-35.
23. Thomas RK, Kallenborn A, Wickenhauser C, et al. Constitutive expression of c-FLIP in Hodgkin and Reed-Sternberg cells. Am J Pathol 2002; 160: 1521-28.
24. Müschen M, Re D, Brauninger A, et al. Somatic mutations of the CD95 gene in Hodgkin and Reed-Sternberg cells. Cancer Res 2000; 60: 5640-43.
25. Maggio EM, Van Den Berg A, de Jong D, et al. Low frequency of FAS mutations in Reed-Sternberg cells of Hodgkin's lymphoma. Am J Pathol 2003; 162: 29-35.
26. Foss HD, Anagnostopoulos I, Araujo I, et al. Anaplastic large-cell lymphomas of T-cell and null-cell phenotype express cytotoxic molecules. Blood 1996; 88: 4005-11.
27. Carbone A, Gloghini A, Gattei V, et al. Reed-Sternberg cells of classical Hodgkin's disease react with the plasma cell-specific monoclonal antibody B-B4 and express human syndecan-1. Blood 1997; 89: 3787-94.
28. Pinkus GS, Pinkus JL, Langhoff E, et al. Fascin, a sensitive new marker for Reed-Sternberg cells of hodgkin's disease. Evidence for a dendritic or B cell derivation? Am J Pathol 1997; 150: 543-62.
29. Delabie J, Shipman R, Bruggen, J et al. Expression of the novel intermediate filament-associated protein restin in Hodgkin's disease and anaplastic large-cell lymphoma. Blood 1992; 80: 2891-96.
30. van den Berg A, Visser L, Poppema S. High expression of the CC chemokine TARC in Reed-Sternberg cells. A possible explanation for the characteristic T-cell infiltratein Hodgkin's lymphoma. Am J Pathol 1999; 154: 1685-91.
31. Jundt F, Anagnostopoulos I, Forster R, et al. Activated Notch1 signaling promotes tumor cell proliferation and survival in Hodgkin and anaplastic large cell lymphoma. Blood 2002; 99: 3398-403.
32. Küppers R, Klein U, Schwering I, et al. Identification of Hodgkin and Reed-Sternberg cell-specific genes by gene expression profiling. J Clin Invest 2003; 111: 529-37.
33. Foss HD, Reusch R, Demel G, et al. Frequent expression of the B-cell-specific activator protein in Reed-Sternberg cells of classical Hodgkin's disease provides further evidence for its B-cell origin. Blood 1999; 94: 3108-13.
34. Hertel CB, Zhou XG, Hamilton-Dutoit SJ, et al. Loss of B cell identity correlates with loss of B cell-specific transcription factors in Hodgkin/Reed-Sternberg cells of classical Hodgkin lymphoma. Oncogene 2002; 21: 4908-20.
35. Hanahan D, Weinberg RA. The hallmarks of cancer. Cell 2000; 100: 57-70.
36. Bargou RC, Leng C, Krappmann D, et al. High-level nuclear NF-kappa B and Oct-2 is a common feature of cultured Hodgkin/Reed-Sternberg cells. Blood 1996; 87: 4340-47.
37. Bargou RC, Emmerich F, Krappmann D, et al. Constitutive nuclear factor-kappaB-RelA activation is required for proliferation and survival of Hodgkin's disease tumor cells. J Clin Invest 1997; 100: 2961-69.
38. Hinz M, Lemke P, Anagnostopoulos I, et al. Nuclear factor kappaB-dependent gene expression profiling of Hodgkin's disease tumor cells, pathogenetic significance, and link to constitutive signal transducer and activator of transcription 5a activity. J Exp Med 2002; 196: 605-17.
39. Emmerich F, Meiser M, Hummel M, et al. Overexpression of I kappa B alpha without inhibition of NF-kappaB activity and mutations in the I kappa B alpha gene in Reed-Sternberg cells. Blood 1999; 94: 3129-34.
40. Cabannes E, Khan G, Aillet F, et al. Mutations in the IkBa gene in Hodgkin's disease suggest a tumour suppressor role for IkappaBalpha. Oncogene 1999; 18: 3063-70.
41. Jungnickel B, Staratschek-Jox A, Bräuninger A, et al. Clonal deleterious mutations in the IkappaBalpha gene in the malignant cells in Hodgkin's lymphoma. J Exp Med 2000; 191: 395-402.
42. Joos S, Kupper M, Ohl S, et al. Genomic imbalances including amplification of the tyrosine kinase gene JAK2 in CD30+ Hodgkin cells. Cancer Res 2000; 60: 549-52.
43. Joos S, Menz CK, Wrobel G, et al. Classical Hodgkin lymphoma is characterized by recurrent copy number gains of the short arm of chromosome 2. Blood 2002; 99: 1381-87.
44. Martin-Subero JI, Gesk S, Harder L, et al. Recurrent involvement of the REL and BCL11A loci in classical Hodgkin lymphoma. Blood 2002; 99: 1474-77.
45. Horie R, Watanabe T, Morishita Y, et al. Ligand-independent signaling by overexpressed CD30 drives NF-kappaB activation in Hodgkin-Reed-Sternberg cells. Oncogene 2002; 21: 2493-503.
46. Annunziata CM, Safiran YJ, Irving SG, et al. Hodgkin disease: pharmacologic intervention of the CD40-NF kappa B pathway by a protease inhibitor. Blood 2000; 96: 2841-48.
47. Fiumara P, Snell V, Li Y, et al. Functional expression of receptor activator of nuclear factor kappaB in Hodgkin disease cell lines. Blood 2001; 98: 2784-90.
48. Kube D, Holtick U, Vockerodt M, et al. STAT3 is constitutively activated in Hodgkin cell lines. Blood 2001; 98: 762-70.
49. Skinnider BF, Elia AJ, Gascoyne RD, et al. Signal transducer and activator of transcription 6 is frequently activated in Hodgkin and Reed-Sternberg cells of Hodgkin lymphoma. Blood 2002; 99: 618-26.
50. Kapp U, Yeh WC, Patterson B, et al. Interleukin 13 is secreted by and stimulates the growth of Hodgkin and Reed-Sternberg cells. J Exp Med 1999; 189: 1939-46.
51. Mathas S, Hinz M, Anagnostopoulos I, et al. Aberrantly expressed c-Jun and JunB are a hallmark of Hodgkin lymphoma cells, stimulate proliferation and synergize with NF-kappa B. EMBO J 2002; 21: 4104-13.
52. Mueller N. Hodgkin's disease. In: Schnottenfeld D, Fraumeni J (Eds). Cancer epidemiology and prevention, Vol 2. New York: Oxford University Press, 1992: 877.
53. Mack TM, Cozen W, Shibata DK, et al. Concordance for Hodgkin's disease in identical twins suggesting genetic susceptibility to the young-adult form of the disease. N Engl J Med 1995; 332: 413-18.
54. Mueller N, Evans A, Harris NL, et al. Hodgkin's disease and Epstein-Barr virus. Altered antibody pattern before diagnosis. N Engl J Med 1989; 320: 689-95.
55. Weiss LM, Strickler JG, Warnke RA, et al. Epstein-Barr viral DNA in tissues of Hodgkin's disease. Am J Pathol 1987; 129: 86-91.
56. Pallesen G, Hamilton-Dutoit SJ, Rowe M, et al. Expression of Epstein-Barr virus latent gene products in tumour cells of Hodgkin's disease. Lancet 1991; 337: 320-22.
57. Herbst H, Dallenbach F, Hummel M, et al. Epstein-Barr virus latent membrane protein expression in Hodgkin and Reed-Sternberg cells. Proc Natl Acad Sci USA 1991; 88: 4766-70.
58. Niedobitek G, Kremmer E, Herbst H, et al. Immunohistochemical detection of the Epstein-Barr virus-encoded latent membrane protein 2A in Hodgkin's disease and infectious mononucleosis. Blood 1997; 90: 1664-72.
59. Gires O, Zimber-Strobl U, Gonnella R, et al. Latent membrane protein 1 of Epstein-Barr virus mimics a constitutively active receptor molecule. EMBO J 1997; 16: 6131-40.
60. Caldwell RG, Wilson JB, Anderson SJ, et al. Epstein-Barr virus LMP2A drives B cell development and survival in the absence of normal B cell receptor signals. Immunity 1998; 9: 405-11.
61. Staratschek-Jox A, Kotkowski S, Belge G, et al. Detection of Epstein-Barr virus in Hodgkin-Reed-Sternberg cells: no evidence for the persistence of integrated viral fragments in Latent membrane protein-1 (LMP-1)-negative classical Hodgkin's disease. Am J Pathol 2000; 156: 209-16.
62. Jarrett RF, Lake A, Andrew L, et al. Somatic IκBα mutations are a frequent occurence in Hodgkin's lymphoma. Blood 2002; 100: 4333 (abstr)
63. Müschen M, Rajewsky K, Krönke M, et al. The origin of CD95-gene mutations in B-cell lymphoma. Trends Immunol 2002; 23: 75-80.
64. Straus SE, Jaffe ES, Puck JM, et al. The development of lymphomas in families with autoimmune lymphoproliferative syndrome with germline Fas mutations and defective lymphocyte apoptosis. Blood 2001; 98: 194-200.
65. Montesinos-Rongen M, Roers A, Küppers R, et al. Mutation of the p53 gene is not a typical feature of Hodgkin and Reed-Sternberg cells in Hodgkin's disease. Blood 1999; 94: 1755-60.
66. Trümper L, Pfreundschuh M, Jacobs G, et al. N-ras genes are not mutated in Hodgkin and Reed-Sternberg cells: results from single cell polymerase chain-reaction examinations. Leukemia 1996; 10: 727-30.
67. Seitz V, Hummel M, Anagnostopoulos I, et al. Analysis of BCL-6 mutations in classic Hodgkin disease of the B- and T-cell type. Blood 2001; 97: 2401-05.
68. Pasqualucci L, Migliazza A, Fracchiolla N, et al. BCL-6 mutations in normal germinal center B cells: evidence of somatic hypermutation acting outside Ig loci. Proc Natl Acad Sci USA 1998; 95: 11816-21.
69. Re D, Benenson E, Wolf J, et al. Lack of BCL10 mutations in Hodgkin's disease-derived cell lines. Br J Haematol 2000; 109: 420-22.
70. Re D, Benenson L, Wickenhauser C, et al. Proficient mismatch repair protein expression in Hodgkin and Reed Sternberg cells. Int J Cancer 2002; 97: 205-10.
71. Hasse U, Tinguely M, Leibundgut EO, et al. Clonal loss of heterozygosity in microdissected Hodgkin and Reed-Sternberg cells. J Natl Cancer Inst 1999; 91: 1581-83.
72. Staratschek-Jox A, Thomas RK, Zander T, et al. Loss of heterozygosity in the Hodgkin-Reed Sternberg cell line L1236. Br J Cancer 2001; 84: 381-87.
73. Re D, Starostik P, Massoudi N, et al. Allelic losses on chromosome 6q25 in Hodgkin and Reed Sternberg cells. Cancer Res 2003; 63: 2606-09.
74. Gaidano G, Hauptschein RS, Parsa NZ, et al. Deletions involving two distinct regions of 6q in B-cell non-Hodgkin lymphoma. Blood 1992; 80: 1781-87.
75. Kupper M, Joos S, von Bonin F, et al. MDM2 gene amplification and lack of p53 point mutations in Hodgkin and Reed-Sternberg cells: results from single-cell polymerase chain reaction and molecular cytogenetic studies. Br J Haematol 2001; 112: 768-75.
76. Alizadeh AA, Eisen MB, Davis RE, et al. Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling. Nature 2000; 403: 503-11.